It has previously been shown (by this inventor) that the bacterium Okadaella gastrococcus (Og) directly contributes to the etiology of gastro-duodenitis and ulcerations in a manner similar to Helicobacter pylori (Hp). U.S. Pat. No. 6,261,824, entitled “Gram Negative Coccoid Bacterium Okadaella Gastrococcus”, which is hereby incorporated by reference in its entirety, discloses the characteristics of this newly isolated bacterium, and methods of detecting its presence in an infected patient. The inventor has now made the discovery that Og is directly contributory to a variety of diseases and disorders in a patient, such as the etiology of cancer in various tissues and organs. Og can also co-exist with Hp in a patient's bodily tissue and fluids-[Og(+)/Hp(+)], or it can exist alone-[Og(+)/Hp(−)].
There are approximately 1.2 million new cases of cancer in the world per year. An overwhelming body of evidence indicates that certain types of pathogens (viruses and bacteria) play a direct role in the etiology of cancers, and that up to 15% of malignancies worldwide are attributable to infections. Although the mechanism involved in most cases remains unclear, one dominant theory is that genetic factors may predispose patients to “cancer causing” bacterial infections, and that infections cause chronic inflammation, as well as immune invasion and suppression. Bacterial infections linked to cancer include: Salmonella typhi to gallbladder cancer; Streptococcus bovis to colon cancer; Chlamydophila pneumoniae to lung cancer; and Helicobacter pylori (Hp) to gastric cancer and mucosa-associated lymphoid tissue (MALT) lymphoma (Mager, D. L., 2006).
Gastric cancer is the fourth most common cancer worldwide, and the second leading cause of cancer related deaths. Hp is now recognized as the primary cause of gastric cancer wherein gastric infection of Hp leads to a 2.1-6.7 increased cancer risk. It has therefore been designated a class 1 carcinogen. In Western countries, e.g. USA and Europe, the incidence of Hp infection is declining, and is presently believed to infect about 30% of the population. The concurrent incidence of distal gastric cancer in this population is about 0.1-1.0%. In Asian countries, such as China and Japan, the Hp infection rate is 60-80% of the population, with a particularly high mortality rate from gastric cancer in Japan that is believed to be due to an extremely virulent Hp strain (Prinz et al, 2006).
Hp and Og infections are not limited to the gastrointestinal system. There is now emerging scientific evidence that both may be involved in the etiology of cancer in non-gastric tissues and organs. In a study involving 43 patients with non-small cell lung cancer, the Hp IgG antibody count was significantly higher in cancer patients than in control groups (Ece et al, 2005). And other research groups have reported that infection with certain Hp strains may lead to a 21-fold increase in relative risk for the development of lung cancer (Prinz et al, 2006). There have also been assertions that Helicobacter subspecies (spp.) microorganisms of various strains have been detected in bodily tissues and fluids located throughout the body (See US patent application 20060078919, entitled “Diagnostic Test Kit and Methods of Diagnosis and Treatment of Helicobacter Spp Associated Infections”). For example, 20060078919 discloses that Helicobacter spp. has been detected in a feline oral lesional mass of cancer cells; in a case of human tongue invasive squamous cell carcinoma; surrounding an osteocarcinoma in a canine leg; in malignant melanoma of a feline eyelid; and in the left ventricle heart muscle cells in a human with myocardial degeneration.
There is therefore a need within the medical community for determining the contributory factor of the bacterial strain Og in the etiology of a disease state, such as cancer. This assessment would also include determining the relative risk of a patient developing gastric and non-gastric cancer as a result of this infection.
There is also a need for efficacious therapeutic treatments to significantly reduce or eradicate Og detected in various fluids, tissues, and organs of a patient who is Og(+)/Hp(+) or Og(+)/Hp(−). This is based on evidence from previous studies that have shown that blocking pathogen proliferation in a disease state, such as cancer, contributed to a successful therapeutic outcome, especially if administered prior to a “point-of-no-return” or a pre-cancerous state.